ArticleCell death and differentiation2016
Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Scalable context-dependent single-cell eQTL mapping reveals disease-relevant regulatory variation beyond static models.medRxiv : the preprint server for health sciences · 2026Article
- Potential targets of baicalein in macrophages revealed by bulk and single cell RNA sequencing analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Contribution of A1 to macrophage survival in cooperation with MCL-1 and BCL-XCell death & disease · 2024Article
- STIM-mediated calcium influx regulates maintenance and selection of germinal center B cells.The Journal of experimental medicine · 2024Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023Review
- Construction of three-gene-based prognostic signature and analysis of immune cells infiltration in children and young adults with B-acute lymphoblastic leukemia.Molecular genetics & genomic medicine · 2022Article
- Recognition of Immune Cell Markers of COVID-19 Severity with Machine Learning Methods.BioMed research international · 2022Article
- Integrated analysis of patient samples identifies biomarkers for venetoclax efficacy and combination strategies in acute myeloid leukemia.Nature cancer · 2020Article
- Transcription factors IRF8 and PU.1 are required for follicular B cell development and BCL6-driven germinal center responses.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Anti-apoptotic A1 is not essential for lymphoma development in Eµ-Myc mice but helps sustain transplanted Eµ-Myc tumour cells.Cell death and differentiation · 2018Article
- Anti-apoptotic BCL-2 family members in development.Cell death and differentiation · 2018Review
- DNA-binding of the Tet-transactivator curtails antigen-induced lymphocyte activation in mice.Nature communications · 2017Article
- MYC selects against reduced BCL2A1/A1 protein expression during B cell lymphomagenesis.Oncogene · 2017Article
- The BCL-2 pro-survival protein A1 is dispensable for T cell homeostasis on viral infection.Cell death and differentiation · 2017Article
- Characterisation of mice lacking all functional isoforms of the pro-survival BCL-2 family member A1 reveals minor defects in the haematopoietic compartment.Cell death and differentiation · 2017Article
- Functional disparities among BCL-2 members in tonsillar and leukemic B-cell subsets assessed by BH3-mimetic profiling.Cell death and differentiation · 2017Article
- Manipulation of Neutrophils byFrontiers in cellular and infection microbiology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Bcl2 family proteins control mitochondrial apoptosis and its members exert critical cell type and differentiation stage-specific functions, acting as barriers against autoimmunity or transformation. Anti-apoptotic Bcl2a1/Bfl1/A1 is frequently deregulated in different types of blood cancers in humans but its physiological role is poorly understood as quadruplication of the Bcl2a1 gene locus in mice hampers conventional gene targeting strategies. Transgenic overexpression of A1, deletion of the A1-a paralogue or constitutive knockdown in the hematopoietic compartment of mice by RNAi suggested rate-limiting roles in lymphocyte development, granulopoiesis and mast cell activation. Here we report on the consequences of conditional knockdown of A1 protein expression using a reverse transactivator (rtTA)-driven approach that highlights a critical role for this Bcl2 family member in the maintenance of mature B-cell homeostasis. Furthermore, we define the A1/Bim (Bcl-2 interacting mediator of cell death) axis as a target of key kinases mediating B-cell receptor (BCR)-dependent survival signals, such as, spleen tyrosine kinase (Syk) and Brutons tyrosine kinase (Btk). As such, A1 represents a putative target for the treatment of B-cell-related pathologies depending on hyperactivation of BCR-emanating survival signals and loss of A1 expression accounts, in part, for the pro-apoptotic effects of Syk- or Btk inhibitors that rely on the 'BH3-only' protein Bim for cell killing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.